05668nam 2201633z- 450 991036756490332120231214133710.03-03921-390-3(CKB)4100000010106097(oapen)https://directory.doabooks.org/handle/20.500.12854/45331(EXLCZ)99410000001010609720202102d2019 |y 0engurmn|---annantxtrdacontentcrdamediacrrdacarrierDNA Replication StressMDPI - Multidisciplinary Digital Publishing Institute20191 electronic resource (368 p.)3-03921-389-X This Special Issue of International Journal of Molecular Sciences (IJMS) is dedicated to the mechanisms mediated at the molecular and cellular levels in response to adverse genomic perturbations and DNA replication stress. The relevant proteins and processes play paramount roles in nucleic acid transactions to maintain genomic stability and cellular homeostasis. A total of 18 articles are presented which encompass a broad range of highly relevant topics in genome biology. These include replication fork dynamics, DNA repair processes, DNA damage signaling and cell cycle control, cancer biology, epigenetics, cellular senescence, neurodegeneration, and aging. As Guest Editor for this IJMS Special Issue, I am very pleased to offer this collection of riveting articles centered on the theme of DNA replication stress. The blend of articles builds upon a theme that DNA damage has profound consequences for genomic stability and cellular homeostasis that affect tissue function, disease, cancer, and aging at multiple levels and through unique mechanisms. I thank the authors for their excellent contributions, which provide new insight into this fascinating and highly relevant area of genome biology.Werner SyndromeA549 cellsepigeneticneurodegenerationGenome integrityadaptationcellular senescencegenome instabilityWerner Syndrome Proteinlipofuscincell cycle checkpointsexonuclease 1template-switchingenergy metabolismmutation frequencyDNA replicationfork regressionmotor neuron diseaseMicrosatellitesAlzheimer's diseasechromatin remodelerrepair of DNA damageAP site analoguemutagensreplication timingThermococcus eurythermalisnucleolar stressgene expressionmutations spectraorigin firingFanconi Anemiasuperfamily 2 ATPaseDNA translocationDNA repairSSB signalinghomologous recombinationcommon fragile sites8-chloro-adenosinereplicationgenome stabilitymutagenicityfork reversalmultiple sclerosisnon-B DNAprotein stabilityheterogeneityubiquitinSenTraGorTM (GL13)replication restartEdU?-arrestinNERagingSSB end resectionoxidative stressATRdormant originsR loopsDNA damage responseDifficult-to-Replicate SequencesDNA double-strand repairendonuclease IVALSdouble strand break repairpremature agingreplication stressEXO1POL?translesion synthesisstrand displacementsG2-arrestDNA replication patternSSB repairgenome integrityG protein-coupled receptor kinase interacting protein 2 (GIT2)MMRreplicative stresssenolyticsspacerinteractomeATR-Chk1 DDR pathwayC9orf72replication fork restarttranslesion DNA synthesisDNA damagemismatch repairDNA replication stressDNA helicasePolymerase kappaDNA fiber assayH1299 cellsTLSAPE2ageingcell deathchromosomeTopBP1barleyclock proteinspost-translational modification8-oxoGS phaseataxia telangiectasia mutated (ATM)G protein-coupled receptor (GPCR)Polymerase etacancerG protein-coupled receptor kinase (GRK)helicasegenomic instabilityParkinson's diseasenucleotide excision repairSupFBrosh Jr Robert Mauth1332974BOOK9910367564903321DNA Replication Stress3041176UNINA